The present invention relates to cardiac devices in general, and more specifically to passive and active cardiac girdles.
Patients having a heart condition known as ventricular dilatation are in a clinically dangerous condition when the patients are in an end stage cardiac failure pattern. The ventricular dilatation increases the load on the heart (that is, it increases the oxygen consumption by the heart), while at the same time decreasing cardiac efficiency. A significant fraction of patients in congestive heart failure, including those who are not in immediate danger of death, lead very limited lives. This dilatation condition does not respond to current pharmacological treatment. A small amount, typically less than 10%, of the energy and oxygen consumed by the heart, is used to do mechanical work. Thus the balance, which is the major part of the energy consumed by the heart is used in maintaining the elastic tension of the heart muscles for a period of time. With a given pressure, the elastic tension is directly proportional to the radius of curvature of the heart ventricle. During ventricular dilatation the ventricular radius increases and the energy dissipated by the heart muscle just to maintain this elastic tension during diastole is abnormally increased, thereby increasing oxygen consumption.
A number of methods and devices have been employed to aid the pumping action of failing hearts. Many of these include sacs or wraps placed around the ailing heart, or, in some instances only around the ventricle of the failing heart, with these wraps constructed to provide for active pumping usually, but not always, in synchronism with the ventricular pumping of the natural heart. A number of cardiac assist systems employing a variety of pumping approaches for assisting the pumping action of a failing natural heart have been developed. These systems include those suitable for partial to full support of the natural heart, short term (a few days) to long term (years), continuous pumping to various degrees of pulsability, and blood contacting versus non-blood contacting. Table 1 lists a number of presently developed devices with pertinent operating characteristics.
One, more recent development in the field of cardiomyoplasty involves the wrapping and pacing of a skeletal muscle around the heart to aid in the pumping. In that configuration, a pacemaker is implanted to control the timing of the activation of the wrapped around skeletal muscle.
A major consideration in the design of cardiac support systems is the risk of thromboembolism. This risk is most associated with use of artificial blood contacting surfaces. A variety of approaches have been employed to reduce or eliminate this problem. One approach has been the employment of smooth surfaces to eliminate potential sites for thrombi and emboli generation as well as textured surfaces to promote cell growth and stabilization of biologic surfaces. One problem affecting thromboembolism risk in heart assists arises from the use of prosthetic, biologic or mechanical pericardial valves. This risk can be some what lowered by the use of anticoagulation therapy. However, the use requires careful manipulation of the coagulation system to maintain an acceptable balance between bleeding and thromboembolic complications. The textured surface approach employs textured polyurethane surfaces and porcine valves to promote pseudo-intima formation with a stable cellular lining. While thromboembolic rates resulting from these measures are acceptable as temporary measures, improvements, particularly for implantable devices are highly desirable.
A second problem associated with implanted cardiac assist devices Is the problem of infection, particularly where the implanted device has large areas of material in contact with blood and tissue. More recently clinical protocols have improved and even the drive line and vent tubes associated with implants that require some percutaneous attachments have been manageable. However, for a ventricular assist device, quality of life considerations require that vent lines and drive lines which cross the skin barrier be eliminated thereby avoiding the encumbrance to patient activities.
A third problem area in ventricular assist devices is the calcification of these devices. This is particularly so for long term implant situations which may last five years or more. Here again the criticality of this factor is reduced for devices which do not involve direct blood contact.
Another approach employed in ventricular assist has been the development of non-pulsatile pumps. However, once again, the blood is exposed to the surfaces of the pump, particularly the bearing and seal area.
Unlike an entirely artificial heart, in which failure of the system leads to death, a ventricular assist device augments the impaired heart and stoppages should not result in death, unless the heart is in complete failure. However, for most present ventricular assist device systems, stoppage of even a few minutes results in formation of blood clots in the device, rendering any restart of the system a very risky undertaking.
According to one aspect, the present invention an artificial myocardium is constructed of an extremely pliant, non-distensible and thin material which can be wrapped around the ventricles of a natural, but diseased heart. This artificial myocardium mimics the contraction-relaxation characteristics of the natural myocardium and provides sufficient contractility, when actuated, to at least equal the contractility of a healthy natural myocardium. In this arrangement all of the direct blood contact is with the interior surfaces of the natural heart and surrounding blood vessel system. The device is hydraulically actuated in timed relationship to the contractions of the natural heart.
Using this system, the natural heart is left in place and the assist system supplies the reinforcing contractile forces required for satisfactory ventricular ejection.
A key concept for this artificial myocardium system is achieved by the realization of a controllable, artificial myocardium employing a cuff formed of a series of closed tubes connected along their axially extending walls. With sufficient hardware to hydraulically (or pneumatically) inflate and deflate these tubes, a controlled contraction is produced as a result of the geometric relationship between the length of these series of tubes in deflated condition and the length of the series of tubes when they are fluidically filled in the inflated condition. If the cuff is formed of a series of xe2x80x9cnxe2x80x9d tubes, each of diameter xe2x80x9cdxe2x80x9d when inflated, connected in series, the total perimeter length of this cuff when deflated is given by n(xcfx80d/2). However, when these tubes are filled with fluid, they have a circular cross-section such that the length of the cuff is the sum of the diameters in the individual tubes or nd. Thus the ratio of the change in perimeter length between the collapsed and the filled state is xcfx80/2. If this cuff is wrapped around the natural heart, it will, when pressurized, shorten and squeeze the heart by producing a xe2x80x9cdiastolicxe2x80x9d to xe2x80x9csystolicxe2x80x9d length change of 36%. Typical sarcomere length changes are approximately 20%.
Suitable hardware, including a hydraulic pump, a compliant reservoir and rotary mechanical valve, together with appropriate actuating electronics can all be implanted in the patient""s body. If the power source is an internal battery, then power may be transcutaneously transmitted into the body to recharge this battery.
Ventricular dilatation is a clinically dangerous condition for end stage cardiac failure patients. The output of the heart is effected by: (a) end-diastolic volume (ventricular volume at the end of the filling- phase), (b) end-systolic volume (ventricular volume at the end of the ejection phase), and (c) heart rate. When (a) is very large, (b) also tends to be larger and (c) tends to be larger than normal. All three of these factors contribute to large increases in the tension-time integral and therefore to increased oxygen consumption.
Only a small amount of the energy consumed by the heart is used to do mechanical work. For example, with a cardiac output of 5 liters/minute, and xcex94p of 100 mm(Hg), the mechanical work done by the left ventricle is about 1.1 watts, and that of the right ventricle is about 0.2 watts. This compares with the typical total energy consumed by the heart (mechanical work during systole plus the energy cost in maintaining elastic tension during diastole) of about 12 to 15 watts.
Thus, since cardiac efficiency (typically between 3% and 15%) is defined as the ratio of the mechanical work done by the heart to the total energy (or load of the heart muscle): then,
Cardiac Efficiency,   η  =            ∫                        P          v                ⁢                  ⅆ          V                                    ∫                  P          ⁢                      ⅆ            V                              +              k        ⁢                  ∫                      xe2x80x83                    ⁢                      T            ⁢                          ⅆ              r                                          
where
Pv: Ventricle Pressure
P: Pressure
V: Volume
T: Tension
t: Time
The constant k accounts for conversion of units.
An increase in mechanical work by a large factor results in a small increase in oxygen consumption but an increase in tension time causes a large increase in oxygen consumption. Patients with dilated ventricles who have undergone active cardiomyoplasty have not been reported to show any objectively measurable hemodynamic improvement.
According to a further aspect of the present invention, a completely: passive girdle is wrapped around the ventricle or the entire heart muscle, and sized so that: it constrains the dilatation during diastole and does not effect the action of the ventricle during: systole. With the present surgical techniques, it is expected initial access to the heart to place the girdle in position, will require opening the chest. However, it may be possible to locate a girdle in position without thoracotomy. In one embodiment, a synthetic girdle made from material that can limit tension, but is otherwise deformable to conform to the anatomical geometry of the recipient heart is used. This girdle may be adjustable in size and shape over an extended period of time in order to gradually decrease the ventricular dilatation. A second embodiment employs a fluid filled passive wrap constructed of a series of horizontal sections. This provides for a variable volume to be enclosed by the wrap with volume control being obtained by controlling the volume of fluid from an implantable reservoir within the body. In its most preferable form, this passive wrap can be formed of a series of horizontal tubular segments each individually sealed and attached to one another along the long axis of the cylinder. If the cylinders are made of indistensible material, then changing the volume of fluid from the cylinders being in a substantially deflated condition to one where they are partially or fully inflated, decreases the internal perimeter of the wrap or girdle, thereby decreasing the effective radius of the girdle around the heart. Another feature of the invention is a feedback system, wherein sensors, for example, strain gauges, can be built into an indistensible lining to measure its tension and thereby provide automatic feedback to a hydraulic circuit controlling the wrap volume.
To avoid the problem of potential irritability and damage to the external myocardium cells by virtue of the artificial wrap and its long term constraining contact with the myocardium, one embodiment of the invention employs a tissue engineered lining to protect the myocardium. This tissue engineered lining consists of a polymer scaffold seeded with myocardial cells harvested from the patient""s own myocardium using tissue engineering technology. That lining then generates a biological myocardio-interfacing surface and remains firmly attached to the polymer interfacing with the surface from which the wrap is made. Such a lining would integrate biologically to the heart""s myocardial cells in a manner analogous to other devices currently being investigated which use cell scaffolds for in vitro and in vitro tissue engineering.
It is therefore an object of the present invention to produce a ventricular assist device system employing an artificial myocardium placed around the natural heart (extra cardiac assist). This design, then, does not contact the bloodstream eliminating many of the problems discussed above.
It is another object of this invention to provide a ventricular assist device which mimics the action of the natural heart while avoiding the compressive action of the direct mechanical ventricular actuation systems on the epicardium.
It is a further object of this invention to provide an artificial myocardium in which the external fluid being pumped is a fraction of the blood volume pumped by the action of the artificial myocardium.
It is yet another object of this invention to provide a ventricular assist device which is compact, requires relatively low energy input and does not require percutaneous components.
It is a further object of this invention to provide a passive girdle to be wrapped around a heart suffering from ventricular dilatation to limit this dilatation and thus improve the performance characteristics of the heart.
It is another object of this invention to provide a passive girdle or vest which can, over a period of time, have its diameter decreased to effect some decrease in dilatation of the ventricle.
Other objects will become apparent in accordance with the description of the preferred embodiments below.